Improvement of growth hormone response to stimulation in primary aldosteronism with correction of potassium deficiency.
Potassium depletion frequently occurs in primary aldosteronism and has been implicated as the cause of the impaired carbohydrate tolerance frequently associated with this syndrome. Glucose, insulin, and growth hormone regulation were studied in a 42-yr-old, male patient with an aldosterone-secreting adenoma when the patient was potassium-depleted and again after potassium repletion. Potassium repletion was documented by serial body potassium measurements, with an increase in body potassium from 2400 mEq to 2850 mEq after 400 mg spironolactone and 80 mEq supplemental potassium chloride were administered daily for 7 days. Potassium repletion resulted in improvement of the patient's glucose tolerance test, with a decrease in the peak glucose level from 184 mg/100ml to 130 mg/100ml and an increase in the peak insulin level from 46 muU/ml to 85 muU/ml. Intravenous administration of arginine resulted in a subnormal insulin response of 28 muU/ml in the base-line test and an increase to 59 muU/ml after potassium stores were repleted. Growth hormone response to arginine infusion was also initially minimal at 12.5 ng/ml, increasing markedly to 26 ng/ml after potassium replenishment. Insulin-induced hypoglycemia resulted in a depressed growth hormone response of 8 ng/ml when the patient was potassium-deficient, but a normal response of 30 ng/ml after potassium repletion. These observations demonstrate that impairment of both insulin and growth hormone responses to stimulation occur in primary aldosteronism with potassium depletion. These abnormalities may be reversed by potassium repletion.